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The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype

BACKGROUND: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as poten...

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Autores principales: Morgan, Claire, Jenkins, Spencer A., Kynaston, Howard G., Doak, Shareen H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864842/
https://www.ncbi.nlm.nih.gov/pubmed/24358122
http://dx.doi.org/10.1371/journal.pone.0081666
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author Morgan, Claire
Jenkins, Spencer A.
Kynaston, Howard G.
Doak, Shareen H.
author_facet Morgan, Claire
Jenkins, Spencer A.
Kynaston, Howard G.
Doak, Shareen H.
author_sort Morgan, Claire
collection PubMed
description BACKGROUND: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as potential biomarkers for prostate cancer progression but the majority of research has been carried out on individual molecules. OBJECTIVE: To elucidate a panel of biomarkers that may help distinguish dormant prostate cancer from aggressive metastatic disease. METHODS: We analysed the expression of 7 well known AJ and TJ components in cell lines derived from normal prostate epithelial tissue (PNT2), non-invasive (CAHPV-10) and invasive prostate cancer (LNCaP, DU145, PC-3) using gene expression, western blotting and immunofluorescence techniques. RESULTS: Claudin 7, α –catenin and β-catenin protein expression were not significantly different between CAHPV-10 cells and PNT2 cells. However, in PC-3 cells, protein levels for claudin 7, α –catenin were significantly down regulated (−1.5 fold, p = <.001) or undetectable respectively. Immunofluoresence showed β-catenin localisation in PC-3 cells to be cytoplasmic as opposed to membraneous. CONCLUSION: These results suggest aberrant Claudin 7, α – and β-catenin expression and/or localisation patterns may be putative markers for distinguishing localised prostate cancer from aggressive metastatic disease when used collectively.
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spelling pubmed-38648422013-12-19 The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype Morgan, Claire Jenkins, Spencer A. Kynaston, Howard G. Doak, Shareen H. PLoS One Research Article BACKGROUND: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as potential biomarkers for prostate cancer progression but the majority of research has been carried out on individual molecules. OBJECTIVE: To elucidate a panel of biomarkers that may help distinguish dormant prostate cancer from aggressive metastatic disease. METHODS: We analysed the expression of 7 well known AJ and TJ components in cell lines derived from normal prostate epithelial tissue (PNT2), non-invasive (CAHPV-10) and invasive prostate cancer (LNCaP, DU145, PC-3) using gene expression, western blotting and immunofluorescence techniques. RESULTS: Claudin 7, α –catenin and β-catenin protein expression were not significantly different between CAHPV-10 cells and PNT2 cells. However, in PC-3 cells, protein levels for claudin 7, α –catenin were significantly down regulated (−1.5 fold, p = <.001) or undetectable respectively. Immunofluoresence showed β-catenin localisation in PC-3 cells to be cytoplasmic as opposed to membraneous. CONCLUSION: These results suggest aberrant Claudin 7, α – and β-catenin expression and/or localisation patterns may be putative markers for distinguishing localised prostate cancer from aggressive metastatic disease when used collectively. Public Library of Science 2013-12-16 /pmc/articles/PMC3864842/ /pubmed/24358122 http://dx.doi.org/10.1371/journal.pone.0081666 Text en © 2013 Morgan et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Morgan, Claire
Jenkins, Spencer A.
Kynaston, Howard G.
Doak, Shareen H.
The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype
title The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype
title_full The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype
title_fullStr The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype
title_full_unstemmed The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype
title_short The Role of Adhesion Molecules as Biomarkers for the Aggressive Prostate Cancer Phenotype
title_sort role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864842/
https://www.ncbi.nlm.nih.gov/pubmed/24358122
http://dx.doi.org/10.1371/journal.pone.0081666
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